Dietary iodide controls its own absorption through post-transcriptional regulation of the intestinal Na+/I- symporter

Autores
Nicola, Juan Pablo; Reyna-Neyra, Andrea; Carrasco, Nancy; Masini, Ana María
Año de publicación
2012
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Dietary I- absorption in the gastrointestinal tract is the first step in I- metabolism. Given that I- is an essential constituent of the thyroid hormones, its concentrating mechanism is of significant physiological importance. We recently described the expression of the Na+/I- symporter (NIS) on the apical surface of the intestinal epithelium as a central component of the I- absorption system and reported reduced intestinal NIS expression in response to an I--rich diet in vivo. Here, we evaluated the mechanism involved in the regulation of NIS expression by I- itself in enterocytes. Excess I- reduced NIS-mediated I- uptake in IEC-6 cells in a dose- and time-dependent fashion, which was correlated with a reduction of NIS expression at the plasma membrane. Perchlorate, a competitive inhibitor of NIS, prevented these effects, indicating that an increase in intracellular I- regulates NIS. Iodide induced rapid intracellular recruitment of plasma membrane NIS molecules and NIS protein degradation. Lower NIS mRNA levels were detected in response to I- treatment, although no transcriptional effect was observed. Interestingly, I- decreased NIS mRNA stability, affecting NIS translation. Heterologous green fluorescent protein-based reporter constructs revealed a significant repressive effect of the I--targeting NIS mRNA 3′ untranslated region. In conclusion, excess I- downregulates NIS expression in enterocytes by virtue of a complex mechanism. Our data suggest that I- regulates intestinal NIS mRNA expression at the post-transcriptional level as part of an autoregulatory effect of I- on its own metabolism. © 2012 The Authors. The Journal of Physiology © 2012 The Physiological Society.
Fil: Nicola, Juan Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Reyna-Neyra, Andrea. University of Yale. School of Medicine; Estados Unidos
Fil: Carrasco, Nancy. University of Yale. School of Medicine; Estados Unidos
Fil: Masini, Ana María. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Materia
Na/I Symporter
Small Intestine
Iodide Absoption
Postranscriptional Regulation
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/54953
Acceder
id CONICETDig_0bd1e8ee0e135356ecfe14051ac5a81f
oai_identifier_str oai:ri.conicet.gov.ar:11336/54953
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Dietary iodide controls its own absorption through post-transcriptional regulation of the intestinal Na+/I- symporterNicola, Juan PabloReyna-Neyra, AndreaCarrasco, NancyMasini, Ana MaríaNa/I SymporterSmall IntestineIodide AbsoptionPostranscriptional Regulationhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Dietary I- absorption in the gastrointestinal tract is the first step in I- metabolism. Given that I- is an essential constituent of the thyroid hormones, its concentrating mechanism is of significant physiological importance. We recently described the expression of the Na+/I- symporter (NIS) on the apical surface of the intestinal epithelium as a central component of the I- absorption system and reported reduced intestinal NIS expression in response to an I--rich diet in vivo. Here, we evaluated the mechanism involved in the regulation of NIS expression by I- itself in enterocytes. Excess I- reduced NIS-mediated I- uptake in IEC-6 cells in a dose- and time-dependent fashion, which was correlated with a reduction of NIS expression at the plasma membrane. Perchlorate, a competitive inhibitor of NIS, prevented these effects, indicating that an increase in intracellular I- regulates NIS. Iodide induced rapid intracellular recruitment of plasma membrane NIS molecules and NIS protein degradation. Lower NIS mRNA levels were detected in response to I- treatment, although no transcriptional effect was observed. Interestingly, I- decreased NIS mRNA stability, affecting NIS translation. Heterologous green fluorescent protein-based reporter constructs revealed a significant repressive effect of the I--targeting NIS mRNA 3′ untranslated region. In conclusion, excess I- downregulates NIS expression in enterocytes by virtue of a complex mechanism. Our data suggest that I- regulates intestinal NIS mRNA expression at the post-transcriptional level as part of an autoregulatory effect of I- on its own metabolism. © 2012 The Authors. The Journal of Physiology © 2012 The Physiological Society.Fil: Nicola, Juan Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Reyna-Neyra, Andrea. University of Yale. School of Medicine; Estados UnidosFil: Carrasco, Nancy. University of Yale. School of Medicine; Estados UnidosFil: Masini, Ana María. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaWiley Blackwell Publishing, Inc2012-12info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/54953Nicola, Juan Pablo; Reyna-Neyra, Andrea; Carrasco, Nancy; Masini, Ana María; Dietary iodide controls its own absorption through post-transcriptional regulation of the intestinal Na+/I- symporter; Wiley Blackwell Publishing, Inc; The Journal Of Physiology; 590; 23; 12-2012; 6013-60260022-37511469-7793CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://physoc.onlinelibrary.wiley.com/doi/abs/10.1113/jphysiol.2012.241307info:eu-repo/semantics/altIdentifier/doi/10.1113/jphysiol.2012.241307info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:43:51Zoai:ri.conicet.gov.ar:11336/54953instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 09:43:51.386CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Dietary iodide controls its own absorption through post-transcriptional regulation of the intestinal Na+/I- symporter
title Dietary iodide controls its own absorption through post-transcriptional regulation of the intestinal Na+/I- symporter
spellingShingle Dietary iodide controls its own absorption through post-transcriptional regulation of the intestinal Na+/I- symporter
Nicola, Juan Pablo
Na/I Symporter
Small Intestine
Iodide Absoption
Postranscriptional Regulation
title_short Dietary iodide controls its own absorption through post-transcriptional regulation of the intestinal Na+/I- symporter
title_full Dietary iodide controls its own absorption through post-transcriptional regulation of the intestinal Na+/I- symporter
title_fullStr Dietary iodide controls its own absorption through post-transcriptional regulation of the intestinal Na+/I- symporter
title_full_unstemmed Dietary iodide controls its own absorption through post-transcriptional regulation of the intestinal Na+/I- symporter
title_sort Dietary iodide controls its own absorption through post-transcriptional regulation of the intestinal Na+/I- symporter
dc.creator.none.fl_str_mv Nicola, Juan Pablo
Reyna-Neyra, Andrea
Carrasco, Nancy
Masini, Ana María
author Nicola, Juan Pablo
author_facet Nicola, Juan Pablo
Reyna-Neyra, Andrea
Carrasco, Nancy
Masini, Ana María
author_role author
author2 Reyna-Neyra, Andrea
Carrasco, Nancy
Masini, Ana María
author2_role author
author
author
dc.subject.none.fl_str_mv Na/I Symporter
Small Intestine
Iodide Absoption
Postranscriptional Regulation
topic Na/I Symporter
Small Intestine
Iodide Absoption
Postranscriptional Regulation
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Dietary I- absorption in the gastrointestinal tract is the first step in I- metabolism. Given that I- is an essential constituent of the thyroid hormones, its concentrating mechanism is of significant physiological importance. We recently described the expression of the Na+/I- symporter (NIS) on the apical surface of the intestinal epithelium as a central component of the I- absorption system and reported reduced intestinal NIS expression in response to an I--rich diet in vivo. Here, we evaluated the mechanism involved in the regulation of NIS expression by I- itself in enterocytes. Excess I- reduced NIS-mediated I- uptake in IEC-6 cells in a dose- and time-dependent fashion, which was correlated with a reduction of NIS expression at the plasma membrane. Perchlorate, a competitive inhibitor of NIS, prevented these effects, indicating that an increase in intracellular I- regulates NIS. Iodide induced rapid intracellular recruitment of plasma membrane NIS molecules and NIS protein degradation. Lower NIS mRNA levels were detected in response to I- treatment, although no transcriptional effect was observed. Interestingly, I- decreased NIS mRNA stability, affecting NIS translation. Heterologous green fluorescent protein-based reporter constructs revealed a significant repressive effect of the I--targeting NIS mRNA 3′ untranslated region. In conclusion, excess I- downregulates NIS expression in enterocytes by virtue of a complex mechanism. Our data suggest that I- regulates intestinal NIS mRNA expression at the post-transcriptional level as part of an autoregulatory effect of I- on its own metabolism. © 2012 The Authors. The Journal of Physiology © 2012 The Physiological Society.
Fil: Nicola, Juan Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Reyna-Neyra, Andrea. University of Yale. School of Medicine; Estados Unidos
Fil: Carrasco, Nancy. University of Yale. School of Medicine; Estados Unidos
Fil: Masini, Ana María. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
description Dietary I- absorption in the gastrointestinal tract is the first step in I- metabolism. Given that I- is an essential constituent of the thyroid hormones, its concentrating mechanism is of significant physiological importance. We recently described the expression of the Na+/I- symporter (NIS) on the apical surface of the intestinal epithelium as a central component of the I- absorption system and reported reduced intestinal NIS expression in response to an I--rich diet in vivo. Here, we evaluated the mechanism involved in the regulation of NIS expression by I- itself in enterocytes. Excess I- reduced NIS-mediated I- uptake in IEC-6 cells in a dose- and time-dependent fashion, which was correlated with a reduction of NIS expression at the plasma membrane. Perchlorate, a competitive inhibitor of NIS, prevented these effects, indicating that an increase in intracellular I- regulates NIS. Iodide induced rapid intracellular recruitment of plasma membrane NIS molecules and NIS protein degradation. Lower NIS mRNA levels were detected in response to I- treatment, although no transcriptional effect was observed. Interestingly, I- decreased NIS mRNA stability, affecting NIS translation. Heterologous green fluorescent protein-based reporter constructs revealed a significant repressive effect of the I--targeting NIS mRNA 3′ untranslated region. In conclusion, excess I- downregulates NIS expression in enterocytes by virtue of a complex mechanism. Our data suggest that I- regulates intestinal NIS mRNA expression at the post-transcriptional level as part of an autoregulatory effect of I- on its own metabolism. © 2012 The Authors. The Journal of Physiology © 2012 The Physiological Society.
publishDate 2012
dc.date.none.fl_str_mv 2012-12
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/54953
Nicola, Juan Pablo; Reyna-Neyra, Andrea; Carrasco, Nancy; Masini, Ana María; Dietary iodide controls its own absorption through post-transcriptional regulation of the intestinal Na+/I- symporter; Wiley Blackwell Publishing, Inc; The Journal Of Physiology; 590; 23; 12-2012; 6013-6026
0022-3751
1469-7793
CONICET Digital
CONICET
url http://hdl.handle.net/11336/54953
identifier_str_mv Nicola, Juan Pablo; Reyna-Neyra, Andrea; Carrasco, Nancy; Masini, Ana María; Dietary iodide controls its own absorption through post-transcriptional regulation of the intestinal Na+/I- symporter; Wiley Blackwell Publishing, Inc; The Journal Of Physiology; 590; 23; 12-2012; 6013-6026
0022-3751
1469-7793
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://physoc.onlinelibrary.wiley.com/doi/abs/10.1113/jphysiol.2012.241307
info:eu-repo/semantics/altIdentifier/doi/10.1113/jphysiol.2012.241307
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Wiley Blackwell Publishing, Inc
publisher.none.fl_str_mv Wiley Blackwell Publishing, Inc
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 13.13397

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